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Revista Brasileira de Ginecologia E... Dec 2020Thrombocytopenia, defined as platelet count < 150,000 mm, is frequently diagnosed by obstetricians since this parameter is included in routine surveillance during... (Review)
Review
Thrombocytopenia, defined as platelet count < 150,000 mm, is frequently diagnosed by obstetricians since this parameter is included in routine surveillance during pregnancy, with an incidence of between 7 and 12%. Therefore, decisions regarding subsequent examination and management are primordial. While most of the cases are due to physiological changes, as gestational thrombocytopenia, other causes can be related to severe conditions that can lead to fetal or maternal death. Differentiating these conditions might be challenging: they can be pregnancy-specific (pre-eclampsia/HELLP syndrome [hemolysis, elevated liver enzymes, low platelets]), or not (immune thrombocytopenia purpura, thrombotic thrombocytopenic purpura or hemolytic uremic syndrome). Understanding the mechanisms and recognition of symptoms and signs is essential to decide an adequate line of investigation. The severity of thrombocytopenia, its etiology and gestational age dictates different treatment regimens.
Topics: Female; Humans; Pregnancy; Pregnancy Complications, Hematologic; Prenatal Diagnosis; Thrombocytopenia
PubMed: 33348401
DOI: 10.1055/s-0040-1721350 -
Anesthesiology Feb 2022
Review
Topics: Anticoagulants; Disease Management; Heparin; Humans; Preoperative Care; Thrombocytopenia
PubMed: 34910815
DOI: 10.1097/ALN.0000000000004090 -
Blood Nov 2017Thrombocytopenia develops in 5% to 10% of women during pregnancy or in the immediate postpartum period. A low platelet count is often an incidental feature, but it might... (Review)
Review
Thrombocytopenia develops in 5% to 10% of women during pregnancy or in the immediate postpartum period. A low platelet count is often an incidental feature, but it might also provide a biomarker of a coexisting systemic or gestational disorder and a potential reason for a maternal intervention or treatment that might pose harm to the fetus. This chapter reflects our approach to these issues with an emphasis on advances made over the past 5 to 10 years in understanding and managing the more common causes of thrombocytopenia in pregnancy. Recent trends in the management of immune thrombocytopenia translate into more women contemplating pregnancy while on treatment with thrombopoietin receptor agonists, rituximab, or mycophenylate, which pose known or unknown risks to the fetus. New criteria to diagnose preeclampsia, judicious reliance on measurement of ADAMTS13 to make management decisions in suspected thrombotic thrombocytopenic purpura, new evidence supporting the efficacy and safety of anticomplement therapy for atypical hemolytic uremic syndrome during pregnancy, and implications of thrombotic microangiopathies for subsequent pregnancies are evolving rapidly. The goals of the chapter are to help the hematology consultant work through the differential diagnosis of thrombocytopenia in pregnancy based on trimester of presentation, severity of thrombocytopenia, and coincident clinical and laboratory manifestations, and to provide guidance for dealing with some of the more common and difficult diagnostic and management decisions.
Topics: Female; Humans; Platelet Count; Pregnancy; Pregnancy Complications, Hematologic; Thrombocytopenia
PubMed: 28637667
DOI: 10.1182/blood-2017-05-781971 -
Haematologica Jun 2022Several therapeutic agents can cause thrombocytopenia by either immune-mediated or non-immune-mediated mechanisms. Non-immune-mediated thrombocytopenia is due to direct... (Review)
Review
Several therapeutic agents can cause thrombocytopenia by either immune-mediated or non-immune-mediated mechanisms. Non-immune-mediated thrombocytopenia is due to direct toxicity of drug molecules to platelets or megakaryocytes. Immune-mediated thrombocytopenia, on the other hand, involves the formation of antibodies that react to platelet-specific glycoprotein complexes, as in classic drug-induced immune thrombocytopenia (DITP), or to platelet factor 4, as in heparin-induced thrombocytopenia (HIT) and vaccine-induced immune thrombotic thrombocytopenia (VITT). Clinical signs include a rapid drop in platelet count, bleeding or thrombosis. Since the patient's condition can deteriorate rapidly, prompt diagnosis and management are critical. However, the necessary diagnostic tests are only available in specialized laboratories. Therefore, the most demanding step in treatment is to identify the agent responsible for thrombocytopenia, which often proves difficult because many patients are taking multiple medications and have comorbidities that can themselves also cause thrombocytopenia. While DITP is commonly associated with an increased risk of bleeding, HIT and VITT have a high mortality rate due to the high incidence of thromboembolic complications. A structured approach to drug-associated thrombocytopenia/thrombosis can lead to successful treatment and a lower mortality rate. In addition to describing the treatment of DITP, HIT, VITT, and vaccine-associated immune thrombocytopenia, this review also provides the pathophysiological and clinical information necessary for correct patient management.
Topics: Hemorrhage; Heparin; Humans; Platelet Count; Purpura, Thrombocytopenic, Idiopathic; Thrombocytopenia; Thrombosis
PubMed: 35642486
DOI: 10.3324/haematol.2021.279484 -
Translational Research : the Journal of... Nov 2020There are currently no effective substitutes for high intensity therapy with unfractionated heparin (UFH) for cardiovascular procedures based on its rapid onset of... (Review)
Review
There are currently no effective substitutes for high intensity therapy with unfractionated heparin (UFH) for cardiovascular procedures based on its rapid onset of action, ease of monitoring and reversibility. The continued use of UFH in these and other settings requires vigilance for its most serious nonhemorrhagic complication, heparin induced thrombocytopenia (HIT). HIT is an immune prothrombotic disorder caused by antibodies that recognize complexes between platelet factor 4 (PF4) and polyanions such as heparin (H).The pathogenicity of anti-PF4/H antibodies is likely due to the formation of immune complexes that initiate intense procoagulant responses by vascular and hematopoietic cells that lead to the generation of platelet microparticles, monocyte and endothelial cell procoagulant activity, and neutrophil extracellular traps, among other outcomes. The development of anti-PF4/H antibodies after exposure to UFH greatly exceeds the incidence of clinical disease, but the biochemical features that distinguish pathogenic from nonpathogenic antibodies have not been identified. Diagnosis relies on pretest clinical probability, screening for anti-PF4/H antibodies and documentation of their platelet activating capacity. However, both clinical algorithms and test modalities have limited predictive values making diagnosis and management challenging. Given the unacceptable rates of recurrent thromboembolism and bleeding associated with current therapies, there is an unmet need for novel rational nonanticoagulant therapeutics based on the pathogenesis of HIT. We will review recent developments in our understanding of the pathogenesis of HIT and its implications for future approaches to diagnosis and management.
Topics: Anticoagulants; Heparin; Humans; Thrombocytopenia
PubMed: 32417430
DOI: 10.1016/j.trsl.2020.04.014 -
British Journal of Haematology Apr 2017A low platelet count is a frequently encountered haematological abnormality in patients treated in intensive treatment units (ITUs). Although severe thrombocytopenia... (Review)
Review
A low platelet count is a frequently encountered haematological abnormality in patients treated in intensive treatment units (ITUs). Although severe thrombocytopenia (platelet count <20 × 10 /l) can be associated with bleeding, even moderate-degree thrombocytopenia is associated with organ failure and adverse prognosis. The aetiology for thrombocytopenia in ITU is often multifactorial and correcting one aetiology may not normalise the low platelet count. The classical view for thrombocytopenia in this setting is consumption associated with thrombin-mediated platelet activation, but other concepts, including platelet adhesion to endothelial cells and leucocytes, platelet aggregation by increased von Willebrand factor release, red cell damage and histone release, and platelet destruction by the complement system, have recently been described. The management of severe thrombocytopenia is platelet transfusion in the presence of active bleeding or invasive procedure, but the risk-benefit of prophylactic platelet transfusions in this setting is uncertain. In this review, the incidence and mechanisms of thrombocytopenia in patients with ITU, its prognostic significance and the impact on organ function is discussed. A practical approach based on the authors' experience is described to guide management of a critically ill patient who develops thrombocytopenia.
Topics: Biomarkers; Blood Coagulation; Critical Illness; Disease Management; Humans; Incidence; Platelet Count; Prognosis; Thrombocytopenia
PubMed: 27982413
DOI: 10.1111/bjh.14482 -
Journal of Thrombosis and Haemostasis :... Jan 2022Prolonged prothrombin time and thrombocytopenia are common in patients with cirrhosis. These parameters do not reflect the overall hemostatic rebalance or bleeding risk... (Review)
Review
Prolonged prothrombin time and thrombocytopenia are common in patients with cirrhosis. These parameters do not reflect the overall hemostatic rebalance or bleeding risk in the periprocedural setting; however, attempts to correct these parameters remain frequent. We review the literature on periprocedural bleeding risk, bleeding risk factors, and the risk and benefits of hemostatic interventions in patients with cirrhosis. We provide guidance recommendations on evaluating bleeding risk in this patient group and management of hemostatic abnormalities in the periprocedural setting.
Topics: Blood Coagulation; Blood Coagulation Disorders; Hemostasis; Humans; Liver Cirrhosis; Thrombocytopenia
PubMed: 34661370
DOI: 10.1111/jth.15562 -
Anaesthesia, Critical Care & Pain... Apr 2020
Topics: Anticoagulants; Heparin; Humans; Thrombocytopenia
PubMed: 32299756
DOI: 10.1016/j.accpm.2020.03.012 -
British Journal of Haematology May 2019Wiskott Aldrich syndrome (WAS) is a primary immunodeficiency disease resulting in recurrent infections, eczema and microthrombocytopaenia. In its classical form,... (Review)
Review
Wiskott Aldrich syndrome (WAS) is a primary immunodeficiency disease resulting in recurrent infections, eczema and microthrombocytopaenia. In its classical form, significant combined immune deficiency, autoimmune complications and risk of haematological malignancy necessitate early correction with stem cell transplantation or gene therapy. A milder form, X-linked thrombocytopaenia (XLT), shares similar bleeding risk from thrombocytopaenia but is not associated with other significant clinical features and is generally managed conservatively. Here, we detail our approach to the diagnosis and treatment of classical WAS and XLT.
Topics: Autoimmune Diseases; Conservative Treatment; Eczema; Female; Genetic Techniques; Genetic Therapy; Hematopoietic Stem Cell Transplantation; Heterozygote; Humans; Infection Control; Male; Mutation; Risk Factors; Thrombocytopenia; Wiskott-Aldrich Syndrome
PubMed: 30864154
DOI: 10.1111/bjh.15831 -
Clinical Toxicology (Philadelphia, Pa.) Jul 2014Abstract A summary of heparin-induced thrombocytopenia (HIT) is presented. HIT is an adverse drug reaction characterized by thrombocytopenia and a high risk for venous... (Review)
Review
Abstract A summary of heparin-induced thrombocytopenia (HIT) is presented. HIT is an adverse drug reaction characterized by thrombocytopenia and a high risk for venous or arterial thrombosis. The frequency of HIT ranges from 1 to 5% of patients receiving heparin with exact frequencies ranging between specific agents. Interestingly, this immune-mediated syndrome is ironically associated with thrombosis, not bleeding, with thrombin formation playing a major role. It is caused by heparin-dependent, platelet-activating antibodies that identifies a self-protein, PF4, bound to heparin that results in an antibody formation. The resulting platelet activation is associated with increased thrombin generation. Typically, the platelet count fall begins 5-10 days after starting heparin, although a rapid platelet count fall can occur in a patient who has antibodies from recent heparin use. Typical causes of HIT as well as the best diagnostic studies and treatment are discussed in this review. HIT was reviewed using a pubmed™ search; google scholar™ using key words: "Heparin-induced thrombocytopenia"; "heparin", and "drug AND thrombocytopenia."
Topics: Antibodies; Heparin; Humans; Thrombocytopenia
PubMed: 24844576
DOI: 10.3109/15563650.2014.917181